Dysrhythmias

Ahmad Hersi
Consultant Electrophysiologist
Assistant Professor
 •Sinus Tachycardia
• Atrial Tachycardia
• Atrial Flutter
• Atrial Fibrillation
• AVRT
• AVNRT
•Junctional Tachycardia

• Ventricular Tachycardia (VT)

• Ventricular Fibrillation (VF)
• Torsade de point
• Polymorphic VT
 Atrial fibrillation
accounts for 1/3 of all 6%
patient discharges PSVT
with arrhythmia as 6%
principal diagnosis. PVCs 18%
Unspecified
4%
Atrial
Flutter

9% 34%
SSS Atrial
Fibrillation

8%
Conduction
Disease
10% VT
3% SCD

2% VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
 Outline Atrial Fibrillation
Description

‹ Chaotic and disorganized atrial activity

‹ Irregular heartbeat
‹ Can be paroxysmal, persistent or
permanent (chronic)
‹ Most common sustained arrhythmia
‹ Can be symptomatic or asymptomatic
‹ Incidence increases with age
Atrial Fibrillation Demographics by Age
U.S. population Population with AF
x 1000 x 1000

30,000 Population with 500

atrial fibrillation
400
U.S. population
20,000
300

200
10,000

100

0 0
<5 5- 10- 15- 20- 25- 30- 35- 40- 45- 50- 55- 60- 65- 70- 75- 80- 85- 90- >95
9 14 19 24 29 34 39 44 49 54 59 64 69 74 79 84 89 94

Age, yr

Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.

 Atrial Fibrillation

‹ Common and age-dependent

2 - 4% over age 60

‹ Significant risk of stroke

4% per year (Framingham Study)

‹ High risk of embolism with cardioversion

 Incidence of AF

‹ The Framingham Study 1982, New England

Journal of Medicine

‹ Annual Incidence 0.1% Per Year

Atrial Fibrillation: Causes

‹ Cardiac
‹ Non-cardiac
‹ “Lone” atrial fibrillation
Atrial Fibrillation: Cardiac Causes
‹ Hypertensive heart disease
‹ Ischemic heart disease
‹ Valvular heart disease
– Rheumatic: mitral stenosis
– Non-rheumatic: aortic stenosis, mitral regurgitation
‹ Pericarditis
‹ Cardiac tumors: atrial myxoma
‹ Sick sinus syndrome
‹ Cardiomyopathy
– Hypertrophic
– Idiopathic dilated (? cause vs. effect)
‹ Post-coronary bypass surgery
Atrial Fibrillation: Non-Cardiac Causes

‹ Pulmonary
– COPD
– Pneumonia
– Pulmonary embolism

‹ Metabolic
– Thyroid disease: hyperthyroidism
– Electrolyte disorder

‹ Toxic: alcohol (‘holiday heart’ syndrome)

 “Lone” Atrial Fibrillation

‹ Absence of identifiable cardiovascular,

pulmonary, or associated systemic
disease

‹ Approximately 0.8 - 2.0% of patients with

atrial fibrillation (Framingham Study)1

‹ In one series of patients undergoing

electrical cardioversion, 10% had lone AF.2
1 Brand FN. JAMA. 1985;254(24):3449-3453.
2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.
 Forms of AF

– Paroxysmal
‹ Paroxysmal lasting less than 48 hours, transient

– Persistent
‹ An episode of AF lasting greater than 48 hours, which can still be
cardioverted to sinus rhythm

– Permanent
– Inability of pharmacologic or non-pharmacologic methods to restore
sinus rhythm
 Symptoms

‹ Palpitations
‹ Presyncope
‹ Fatigue
‹ Chest pain
‹ Dyspnea
‹ Syncope
 Work-up

‹ EKG
‹ ECHO
‹ TFT
‹ 24 h Holter
‹ Others…..
 ECG Recognition

‹ Atrial Rate: > 300 bpm

‹ Rhythm: Irregular
– Ventricular Rate: Variable
• Dependent upon:
• AV node conduction properties
• Sympathetic and parasympathetic ton

‹ Recognition: Absence of P waves

 Atrial Fibrillation: Clinical Problems
‹ Embolism and stroke (presumably due to LA clot)
‹ Acute hospitalization with onset of symptom
‹ Congestive heart failure
– Loss of AV synchrony
– Loss of atrial “kick”
– Rate-related cardiomyopathy due to rapid ventricular response

‹ Rate-related atrial myopathy and dilatation

‹ Chronic symptoms and reduced sense of well-being
 Management Strategies

‹ Prevention of Thromboembolis

‹ Rate control

‹ Restoration of sinus rhythm

 Therapeutic Approaches to
Atrial Fibrillation
‹ Anticoagulation

‹ Antiarrhythmic suppression

‹ Control of ventricular response

– Pharmacologic

– Catheter modification/ablation of AV node

‹ Curative procedures
– Surgery (maze)

– Catheter ablation
‹ Prevention of Thromboembolis
 Atrial Fibrillation and Stroke

‹ Risk: 5 - 8% per year in high-risk patients

‹ Anticoagulant therapy is clearly indicated and

beneficial in rheumatic atrial fibrillation.

‹ In non-rheumatic atrial fibrillation, major

randomized trials have provided useful
guidelines for identifying and treating patients
at risk.
Predictors of Thromboembolic Risk in
Atrial Fibrillation

‹ Congestive Heart Failure

‹ Hypertension

‹ Age ≥75 years CHADS2

‹ Diabetes

‹ Stroke or TIA
CHADS2 Score and Risk of Stroke

JAMA 2001;285:2864
‹ Restoration of sinus rhythm
 Antiarrhythmic Drugs to Suppress
Atrial Fibrillation

‹ Class I agents
– IA: quinidine, procainamide, disopyramide
– IC: flecainide, propafenone

‹ Class III agents

– amiodarone, sotalol
 Timing of Cardioversion for
Atrial Fibrillation
‹ Chronic
1 month coumadin → cardioversion (CV)

‹ Uncertain duration
Stable → 1 month coumadin → CV
Unstable → TEE → CV

‹ Acute
no clot
CV → coumadin
Heparin → TEE
coumadin → repeat TEE → CV
clot
‹ Rate control
 Control of Ventricular Rate in
Atrial Fibrillation

‹ Digoxin

‹ Calcium channel blockers

Verapamil, diltiazem

‹ Beta blockers
Sinus Tachycardia (ST)
Clinical Conditions Associated with Persistent
Sinus Tachycardia

‹ Fever ‹ Hypoxemia (PE / COPD)

‹ Volume depletion ‹ Cardiac conditions →

decreased cardiac output (CHF
‹ Anemia / MI)

‹ Sepsis (due to profound ‹ Medications (B2 agonists)

vasodilatation → reflex
tachycardia) ‹ Drugs (crack / ephedrine)

‹ Pain / anxiety ‹ Hyperthyroidism

 Rx – Sinus Tachycardia

‹ Sinus tachycardia is almost always a physiologic

response to a given stimulus or disease state

‹ In most situations, do not treat sinus tachycardia,

treat the underlying process
Focal Atrial Tachycardia
 Causes – Atrial Tachycardia

‹ Onset is often precipitated by increased sympathetic

stimulation

‹ Specific examples:
• Digoxin toxicity (especially if AV block noted)
• Theophylline (beta-agonist)
• EtOH
• Myocardial ischemia
• Hypoxia
 Rx – Atrial Tachycardia

‹ Rhythm often spontaneously resolves with

normalization of
sympathetic tone

‹ If rhythm recurs repeatedly, consider Rx:

• Step #1 – beta-blockers (BB)
• Step #2 – amiodarone (not if dig toxic)
• Step #3 – radio-frequency ablation is curative

Kowey PR. Arch Int Med. 1998; 158: 325

Atrial Flutter with 2:1 AV block
 Background - Atrial Flutter

‹ Underlying mechanism – large “macro re-entrant circuit” in the

atrium, typically moves counter-clockwise
‹ Atrial rate range: 250-350 bpm
‹ Ventricular response depends on the degree of AV block:
• 2:1 block → ventricular rate = 150 bpm
• 3:1 block → 100 bpm
• 4:1 block → 75 bpm
 Causes – Atrial Flutter

‹ Most commonly occurs in male patients with dilated or

distended atria with elevated left atrial pressure

‹ Clinical scenarios:
– Systolic CHF with low EF
– Mitral regurgitation (MR)
 Rx – Atrial Flutter

‹ Unstable pt (i.e. low BP / CP / AMS):

• Synchronized cardioversion as per ACLS
• 50J → 100J → 200J → 300J → 360J

‹ Stable pt:
• Rate control - just like atrial fibrillation (AFib)
• Elective cardioversion - just like AFib
• Anti-coagulation – just like AFib
Atrioventricular Nodal Re-entrant
Tachycardia (AVNRT) or AVRT
AVNRT or AVRT
 Rx – AVNRT / AVRT
‹ Unstable:
– Synchronized cardioversion start @ 50J (avoid if EF < 40%)

‹ Stable:
– Step #1 – attempt to terminate rhythm with vagal
maneuvers (carotid
massage / Valsalva)
– Step #2 – adenosine 6mg IVP → 12mg 2min later →
18mg 2min later
– Step #3 – AV nodal blocking agents (BB / CCB > digoxin)
– Step #4 – amiodarone 150mg IV over 10min → 1mg/min
x 6hrs → 0.5mg/min x 18hrs
(max dose
2.2g/24hrs)
– Step #5 – in pts with bypass tracts not tolerating the
medications,
consider radio-frequency ablation

ACLS 2000 / Wang YS, et al. JACC. 1991; 18:1711

Wolf-Parkinson-White (WPW)
Syndrome
 Take Home Messages - WPW
‹ Syndrome features:
• Short PR
• Broad irregular QRS complexes due to Delta waves
• Ventricular rates up to 300 bpm
‹ Conduction along the accessory pathway:
• Orthodromic – conduction to ventricles over normal AV
node-His-Purkinje path
• Antidromic – conduction to ventricles via accessory path
‹ Medical Rx:
• 1st choice – procainamide 20mg/min IV (max 17mg/kg)
• Drugs to avoid – AV nodal blocking agents!!!
• Radio-frequency ablation curative > 95% cases

ACLS 2000 / Krahn AD. Ann Intern Med. 1992; 116: 456
 So What Is Actually Meant By
Supraventricular Tachycardia?

‹ Arrhythmias of supraventricular origin using a re-entrant

mechanism with abrupt onset & termination

‹ AVNRT (60%)

‹ AVRT (30%)

‹ Atrial tachycardia (10%)

Ventricular Tachycardia (VT)
 Brugada EKG Criteria for VT

‹ AV dissociation

‹ R-S interval > 100 ms

‹ No RS morphology in pre-cordial leads

Dr. Brugada (Cardiology) @ Noon Conference – The Methodist Hospital 9/00

 Classification - VT
‹ Duration:
– Sustained VT (> 30 seconds or hemodynamic
compromise)
– non-Sustained VT (< 30 seconds)
• Risk factor for sudden death among pts with heart dz

‹ QRS morphology:
– Monomorphic (common in pts with CAD)
– Polymorphic (usually associated with a prolonged QT)

ACP - MKSAP 12. Cardiovascular Medicine: 24

 Rx – VT

‹ Hemodynamically Unstable:
– Unsynchronized cardioversion as per ACLS protocol for VF /
pulseless VT

‹ Unstable (CP / AMS):

– Synchronized cardioversion as per ACLS protocol
 Rx – VT
‹ Stable:
– Rx ischemia
– Correct electrolytes (K / Mg / Ca)
– Consider cardioversion (yes even in stable pts!!)
– EF > 40%:
• Procainamide / sotalol (class IIa)
• amiodarone (class IIb)
– EF < 40%:
• amiodarone (class IIa)
Torsades de Pointes
 Causes – Torsades de Pointes

‹ Underlying Mechanism – prolongation of the QT interval coupled

with R-on-T phenomenon

‹ Medications (Class Ia anti-arrhythmics / TCAs)

‹ Electrolyte abnormalities (Mg / K)

‹ Bradycardia (usually s/p inferior MI)

 Rx – Torsades de Pointes

‹ Unstable:
• Cardioversion as per ACLS protocol for VT based on
hemodynamics (refer to prior slides)

‹ Stable:
• Correct electrolytes (K / Mg)
• Hold any culprit medications
• magnesium sulfate 2g IVP + repeat prn
• Transcutaneous overdrive pacing
 Summary - Wide

‹ Ventricular tachycardia (VT)

‹ Torsades de Pointes (sub-type of VT)

‹ Any supraventricular tachycardia with aberrancy (e.g. sinus

tach with pre-existing bundle branch block)